Previously, our group verified higher activity of mannose receptors on Selleck Ku 0059436 macrophages from mice

pretreated with Con-A for 3 days compared to control group (Geraldino et al., 2010). In that study, Con-A-activated cells were able to destroy 70% of the C. albicans CR15 inoculum during 1 h of coincubation; however, macrophages from the control group killed only 30% of the pathogen. In this study, a reduction of 50.1 ± 3.6% in Candida phagocytosis was observed in the presence of mannan (100 μg mL−1) and 40.2 ± 3.8% in the presence of laminarin (100 μg mL−1), revealing higher activity of mannose and dectin-1 receptors on Con-A-activated macrophages, but not in PBS-macrophages (Table 1). Owing to the increase in the activity of mannose and dectin-1 receptors,

in this study, it was proposed that these pathways of phagocytosis could be mediating an adaptative immune response involving TH17 cells over the course of mouse infection with Candida. In the Con-A group, a significant increase in IL-17 concentrations occurred at 6 h postinfection that was maintained up to 18 h (Fig. 1). In the control group, analysis verified that the levels of IL-17 were significantly reduced over the course of infection compared to mice pretreated with Con-A (Fig. 1). Therefore, this study demonstrated the possibility that mannose and dectin-1 receptors could signalize click here the differentiation of TH17 cells with IL-17 production in the course of Candida infection in mice pretreated with Con-A. Corroborating these results, Van de Veerdonk et al. (2009) and LeibundGut-Landmann et al. (2007), reported that mannose receptors on human macrophages and dectin-1-activated dendritic cells from mice participate in the differentiation of naïve TCD4+ in effector T cells (TH-17 cells) in vitro in response to C. albicans. Although numerous studies have focused on the pathological aspects of IL-17-producing cells in autoimmune diseases, their role in protective antifungal immunity has also been increasingly Adenosine triphosphate recognized (Conti & Gaffen, 2010;

Rehaume et al., 2010). Thus, our interest was to investigate whether the cytokines TGF-β, IL-1β and IL-6 could be driving the development of TH17 cells. Figure 2a shows basal levels of TGF-β in both groups; however, the levels of this cytokine were significantly higher in mice pretreated with Con-A 2 h postinfection, suggesting a trigger for TH17 differentiation. Corroborating these results, Mangan et al. (2006) demonstrated that TGF-β acted to promote a substantial increase in TH17+ cells independent of IL-23 in an experimental model under IFN-γ-null conditions; furthermore, the development of TH17 cells was impaired in TGF-β1-deficient mice, and also, IL-17 secretion was impaired in a dose-dependent manner when neutralizing antibody to TGF-β or IL-6 were present (Torchinsky et al., 2009). IL-6 production is dependent on signaling by dectin-1 receptor according to LeibundGut-Landmann et al.